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Prostaglandin E receptor EP4 is a therapeutic target in breast cancer cells with stem-like properties

Namita Kundu1, Xinrong Ma, Tyler Kochel

  • 1Department of Pathology, University of Maryland, Baltimore, MD, USA, nkundu@umaryland.edu.

Breast Cancer Research and Treatment
|November 28, 2013
PubMed

Insights

Targeting prostaglandin E receptor 4 (EP4) inhibits breast cancer stem cell properties. EP4 antagonists reduce tumor initiation and stem cell markers, suggesting EP4 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Stem Cell Biology

Background:

  • The cyclooxygenase (COX) pathway is implicated in breast cancer progression.
  • The role of COX pathway in breast cancer stem/progenitor cells is undefined.
  • Prostaglandin E receptor 4 (EP4) is expressed in invasive breast carcinomas and antagonizing it inhibits metastasis.

Purpose of the Study:

  • To define the role of the COX pathway, specifically EP4, in breast cancer stem/progenitor cell biology.
  • To investigate EP4 as a potential therapeutic target for breast cancer stem cells.

Main Methods:

  • Assessed COX-2 and EP4 expression in mammosphere-forming breast cancer cells.
  • Treated mammosphere cells with EP4 inhibitors or EP4 gene silencing.
  • Evaluated tumor-initiating capacity and stem cell markers in vivo using an oral EP4 antagonist.

Main Results:

  • Mammosphere-forming cells with metastatic potential upregulate EP4 and COX-2, exhibiting increased tumorigenicity.
  • EP4 inhibition or silencing reduced mammosphere-forming capacity and stem cell markers.
  • An oral EP4 antagonist reduced tumor initiation and stem cell markers in vivo.

Conclusions:

  • EP4 plays a critical role in supporting the breast cancer stem cell phenotype and tumor-initiating capacity.
  • EP4 antagonism represents a promising therapeutic strategy for targeting breast cancer stem cells.

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